CASE 1
A 13-year-old Quarter Horse gelding used for American sport disciplines
was referred for stranguria of 12 hours’ duration, with a suspect of
intravesical mass.
At first clinical examination, the horse was bright and responsive,
heart rate 36 bpm, respiratory rate 40 bpm, rectal temperature 37.8°C,
normal gut sounds, congested mucous membranes with slightly prolonged
capillary refill time (2”). The horse showed constant urine dripping
from the penis and appeared to experience pain while walking. The owner
reported a sudden increase of muscular masses in the last days. Rectal
palpation and ultrasonography revealed distended urinary bladder with
mucous and viscous hyperechogenic content, enlarged spleen, and no other
abnormalities. Haematology and biochemistry revealed moderate anaemia
(hematocrit 26.5%), moderate azotaemia, mild hyponatremia, and markedly
elevated levels of creatinine kinase (1.750.000 UI). A diagnosis of
myopathy was made, and genetic analysis sent for a panel of
breed-associated disorders. They subsequently revealed a heterozygous
genotype for MYHM (myosin-heavy chain myopathy) gene and
immunosuppressive therapy based on dexamethasone intravenously (IV) at
0,06 mg/kg q24 h for 5 days followed by 1 mg/kg prednisolone PO q24 h,
was then instituted. Treatment with aggressive fluid therapy was
initiated in association with flunixin meglumine IV 1.1 mg/kg q24 h. The
stranguria was ascribed to the unwillingness of the horse to assume
urination position due to muscle pain. The bladder was catheterized
during the first visit and 7 litres of dark urine with sand deposits
were removed. Bladder was washed with sterile saline solution to remove
sabulous detritus. Stranguria persisted in the following days of
hospitalization, despite analgesic treatment, and blood clots in the
urines were observed macroscopically. Ultrasound examination of the
bladder revealed a heterogeneous hyperechogenic mass in ventral portion
of the urinary bladder (Figure 1D). The ventrocaudal part of the wall
appeared thickened (8.4 mm) and oedematous, the rest of the organ
presented a normo-echogenic aspect. At cystoscopy, performed using a
160-cm flexible endoscopec, the bladder mucosa was
hyperaemic with diffuse petechiation and deep ulcers appreciable in the
ventral aspect of the organ (Figure 1A-B). Macroscopically, urine
appeared dark brown to rose in colour, with mucous as well as mucosal
fragments and blood clots in suspension. Urine culture was requested
(which then yielded a E. coli sensitive to
trimethoprim-sulfamethoxazole [TMS]) and an initial treatment with
15 mg/kg ampicillin IV q8 h and 25 mg/kg TMS PO q12 h was started.
Despite clinical improvements, marked bleeding persisted for up to ten
days from the bladder ulcer, with hematocrit gradually decreasing. Local
application of CSP on the bladder mucosa where the ulcer was evident was
attempted under endoscopic guidance. The CSP (5 g) was gently inserted
into a catheter with 1.8mm outer diameter and 190cm
lengthd, which was then passed through the working
channel of the endoscope after bladder emptying. Bleeding from the ulcer
was substantial and margins of the lesion were not identifiable for long
time. The powder was air pushed through the catheter and immediately
created a gel coating over the ulcerated mucosal area. Endoscope was
retracted and urine production closely monitored, as we hypothesized
that the haemostatic clot could move and generate obstruction to urine
outflow. Bladder transrectal ultrasound appearance was also monitored
daily in the following days. Frank bleeding stopped in 24 hours after
CSP application. The horse did not show pain or stranguria at any time
and continue to autonomously void the bladder with the expected
frequency. Ultrasonographically, a hyperecogenic halo was evident in the
ventral portion of the bladder which gradually decreased in size over
the next 7 days, which was interpreted as the clot induced by CSP over
the area of ulcerated mucosa, while the mucosa became hypertrophic
(Figure 1C-E-F). Treatment with TMS was continued for additional 7 days,
when urine cytology and culture were judged negative. A further
ultrasonographic control performed 14 days after the end of
antimicrobial treatment still identified an area of thickened mucosa
(Figure 1G), in the absence of evidence of macro or microhaematuria and
inflammation.